1. Scrutinizing the Expression and Blockade of Inhibitory Molecules Expressed on T Cells from Acute Myeloid Leukemia Patients.
- Author
-
Abdolmaleki M, Mojtabavi N, Zavvar M, Vaezi M, Noorbakhsh F, and Nicknam MH
- Subjects
- Adolescent, Adult, Cell Proliferation, Cells, Cultured, Female, Gene Expression Regulation, Neoplastic, Humans, Immune Tolerance, Immunophenotyping, Lymphocyte Activation, Male, Middle Aged, Signal Transduction, Young Adult, CD4-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes immunology, Hepatitis A Virus Cellular Receptor 2 metabolism, Leukemia, Myeloid, Acute immunology, Programmed Cell Death 1 Receptor metabolism, Signaling Lymphocytic Activation Molecule Family metabolism
- Abstract
T cell exhaustion is an immunosuppressive mechanism which occurs in chronic viral infections, solid tumors and hematologic malignancies. Exhausted T cell has increased the expression of inhibitory receptors, and functional impairment. In this study, we investigated the expression from some of those inhibitory receptors being Programmed death 1 (PD-1), T cell immunoglobulin and mucin domain containing molecules 3 (TIM-3) and CD244 on T cells from Iranian acute myeloid leukemia (AML) patients. Peripheral blood samples were collected from Iranian newly diagnosed AML patients and flow cytometric analysis was accomplished for cell surface expression of PD-1, TIM-3, and CD244 on T lymphocytes. Functionality and proliferation assay were done in the presence of anti-PD-1 and anti-CD244 blocking antibodies. Immunophenotyping of T cells showed a significant increase of PD-1 and CD244 expression on CD4+ and CD8+ T cells of AML patients. Whereas blockade of PD1 and CD244 increased the proliferation of CD4+ and CD8+ T lymphocytes of AML patients but IFN-γ production was not significantly increased. In conclusion, our data indicate that CD4+ and CD8+ T cells from AML patients appeared to be exhausted and blockade of some immune checkpoints can improve the proliferation of those cells.
- Published
- 2018